@article{SunHuangMengetal.2012,
  author    = {Sun, Sheng-Yun and Huang, Jin and Meng, Min-Jie and Lu, Jia-Hai and Hocher, Berthold and Liu, Kang-Li and Yang, Qin-He and Zhu, Xiao-Feng},
  title     = {Improvement of lipid profile and reduction of body weight by Shan He Jian Fei Granules in high fat diet-induced obese rats},
  series = {Clinical laboratory : the peer reviewed journal for clinical laboratories and laboratories related to blood transfusion},
  volume    = {58},
  journal   = {Clinical laboratory : the peer reviewed journal for clinical laboratories and laboratories related to blood transfusion},
  number    = {1-2},
  publisher = {Clin Lab Publ., Verl. Klinisches Labor},
  address   = {Heidelberg},
  issn      = {1433-6510},
  pages     = {81 -- 87},
  year      = {2012},
  abstract  = {Background: The goal was to study lipid profiles (TG, TC, LDL, HDL), effects on serum leptin, and fat tissue adiponectin, and resistin as well as body weight effects of Shan He Jian Fei Granules (SHJFG) in rats on a high fat diet. Methods: Rats were randomly divided into five groups: normal control group fed with normal fat diet, rats on high fat diet receiving low dosage, middle dosage, high dosage of Shan He Jian Fei Granules (SHJFG) as well as a high fat diet group receiving placebo. Rats were treated for 8 weeks. Body weight and naso-anal length of each rat were recorded and Lee's index was calculated. Serum TG, TC, LDL, HDL and leptin concentrations were analyzed. The gene expressions of adiponectin and resistin in adipose tissues were tested by RT-PCR. Results: Compared to the high-fat diet group, body weights, Lee's indexes, weight of fat tissues and serum TG, TC, LDL and leptin of SHJFG groups significantly decreased (p<0.05), whereas mRNA expressions of adiponectin and resistin of SHJFG groups significantly increased (p<0.05). Conclusions: SHJFG could significantly lower body weight and serum TG, TC, and LDL of obese rats. The effects of SHJFG in lowering leptin synthesis and raising mRNA expression of adiponectin and resistin in fat tissues may act as part of the mechanisms in lowering body weight of obese rats. Further studies are needed to demonstrate whether SHJFG may also reduce overall cardiovascular morbidity and mortality like other lipid lowering drugs.},
  language  = {en}
}
@article{ArminChenJinetal.2018,
  author    = {Armin, Ardalan and Chen, Zhiming and Jin, Yaocheng and Zhang, Kai and Huang, Fei and Shoaee, Safa},
  title     = {A Shockley-Type polymer},
  series = {Advanced energy materials},
  volume    = {8},
  journal   = {Advanced energy materials},
  number    = {7},
  publisher = {Wiley-VCH},
  address   = {Weinheim},
  issn      = {1614-6832},
  doi       = {10.1002/aenm.201701450},
  pages     = {9},
  year      = {2018},
  abstract  = {Charge extraction rate in solar cells made of blends of electron donating/accepting organic semiconductors is typically slow due to their low charge carrier mobility. This sets a limit on the active layer thickness and has hindered the industrialization of organic solar cells (OSCs). Herein, charge transport and recombination properties of an efficient polymer (NT812):fullerene blend are investigated. This system delivers power conversion efficiency of >9\% even when the junction thickness is as large as 800 nm. Experimental results indicate that this material system exhibits exceptionally low bimolecular recombination constant, 800 times smaller than the diffusion-controlled electron and hole encounter rate. Comparing theoretical results based on a recently introduced modified Shockley model for fill factor, and experiments, clarifies that charge collection is nearly ideal in these solar cells even when the thickness is several hundreds of nanometer. This is the first realization of high-efficiency Shockley-type organic solar cells with junction thicknesses suitable for scaling up.},
  language  = {en}
}
@article{WuttkeLiLietal.2019,
  author    = {Wuttke, Matthias and Li, Yong and Li, Man and Sieber, Karsten B. and Feitosa, Mary F. and Gorski, Mathias and Tin, Adrienne and Wang, Lihua and Chu, Audrey Y. and Hoppmann, Anselm and Kirsten, Holger and Giri, Ayush and Chai, Jin-Fang and Sveinbjornsson, Gardar and Tayo, Bamidele O. and Nutile, Teresa and Fuchsberger, Christian and Marten, Jonathan and Cocca, Massimiliano and Ghasemi, Sahar and Xu, Yizhe and Horn, Katrin and Noce, Damia and Van der Most, Peter J. and Sedaghat, Sanaz and Yu, Zhi and Akiyama, Masato and Afaq, Saima and Ahluwalia, Tarunveer Singh and Almgren, Peter and Amin, Najaf and Arnlov, Johan and Bakker, Stephan J. L. and Bansal, Nisha and Baptista, Daniela and Bergmann, Sven and Biggs, Mary L. and Biino, Ginevra and Boehnke, Michael and Boerwinkle, Eric and Boissel, Mathilde and B{\"o}ttinger, Erwin and Boutin, Thibaud S. and Brenner, Hermann and Brumat, Marco and Burkhardt, Ralph and Butterworth, Adam S. and Campana, Eric and Campbell, Archie and Campbell, Harry and Canouil, Mickael and Carroll, Robert J. and Catamo, Eulalia and Chambers, John C. and Chee, Miao-Ling and Chee, Miao-Li and Chen, Xu and Cheng, Ching-Yu and Cheng, Yurong and Christensen, Kaare and Cifkova, Renata and Ciullo, Marina and Concas, Maria Pina and Cook, James P. and Coresh, Josef and Corre, Tanguy and Sala, Cinzia Felicita and Cusi, Daniele and Danesh, John and Daw, E. Warwick and De Borst, Martin H. and De Grandi, Alessandro and De Mutsert, Renee and De Vries, Aiko P. J. and Degenhardt, Frauke and Delgado, Graciela and Demirkan, Ayse and Di Angelantonio, Emanuele and Dittrich, Katalin and Divers, Jasmin and Dorajoo, Rajkumar and Eckardt, Kai-Uwe and Ehret, Georg and Elliott, Paul and Endlich, Karlhans and Evans, Michele K. and Felix, Janine F. and Foo, Valencia Hui Xian and Franco, Oscar H. and Franke, Andre and Freedman, Barry I. and Freitag-Wolf, Sandra and Friedlander, Yechiel and Froguel, Philippe and Gansevoort, Ron T. and Gao, He and Gasparini, Paolo and Gaziano, J. Michael and Giedraitis, Vilmantas and Gieger, Christian and Girotto, Giorgia and Giulianini, Franco and Gogele, Martin and Gordon, Scott D. and Gudbjartsson, Daniel F. and Gudnason, Vilmundur and Haller, Toomas and Hamet, Pavel and Harris, Tamara B. and Hartman, Catharina A. and Hayward, Caroline and Hellwege, Jacklyn N. and Heng, Chew-Kiat and Hicks, Andrew A. and Hofer, Edith and Huang, Wei and Hutri-Kahonen, Nina and Hwang, Shih-Jen and Ikram, M. Arfan and Indridason, Olafur S. and Ingelsson, Erik and Ising, Marcus and Jaddoe, Vincent W. V. and Jakobsdottir, Johanna and Jonas, Jost B. and Joshi, Peter K. and Josyula, Navya Shilpa and Jung, Bettina and Kahonen, Mika and Kamatani, Yoichiro and Kammerer, Candace M. and Kanai, Masahiro and Kastarinen, Mika and Kerr, Shona M. and Khor, Chiea-Chuen and Kiess, Wieland and Kleber, Marcus E. and Koenig, Wolfgang and Kooner, Jaspal S. and Korner, Antje and Kovacs, Peter and Kraja, Aldi T. and Krajcoviechova, Alena and Kramer, Holly and Kramer, Bernhard K. and Kronenberg, Florian and Kubo, Michiaki and Kuhnel, Brigitte and Kuokkanen, Mikko and Kuusisto, Johanna and La Bianca, Martina and Laakso, Markku and Lange, Leslie A. and Langefeld, Carl D. and Lee, Jeannette Jen-Mai and Lehne, Benjamin and Lehtimaki, Terho and Lieb, Wolfgang and Lim, Su-Chi and Lind, Lars and Lindgren, Cecilia M. and Liu, Jun and Liu, Jianjun and Loeffler, Markus and Loos, Ruth J. F. and Lucae, Susanne and Lukas, Mary Ann and Lyytikainen, Leo-Pekka and Magi, Reedik and Magnusson, Patrik K. E. and Mahajan, Anubha and Martin, Nicholas G. and Martins, Jade and Marz, Winfried and Mascalzoni, Deborah and Matsuda, Koichi and Meisinger, Christa and Meitinger, Thomas and Melander, Olle and Metspalu, Andres and Mikaelsdottir, Evgenia K. and Milaneschi, Yuri and Miliku, Kozeta and Mishra, Pashupati P. and Program, V. A. Million Veteran and Mohlke, Karen L. and Mononen, Nina and Montgomery, Grant W. and Mook-Kanamori, Dennis O. and Mychaleckyj, Josyf C. and Nadkarni, Girish N. and Nalls, Mike A. and Nauck, Matthias and Nikus, Kjell and Ning, Boting and Nolte, Ilja M. and Noordam, Raymond and Olafsson, Isleifur and Oldehinkel, Albertine J. and Orho-Melander, Marju and Ouwehand, Willem H. and Padmanabhan, Sandosh and Palmer, Nicholette D. and Palsson, Runolfur and Penninx, Brenda W. J. H. and Perls, Thomas and Perola, Markus and Pirastu, Mario and Pirastu, Nicola and Pistis, Giorgio and Podgornaia, Anna I. and Polasek, Ozren and Ponte, Belen and Porteous, David J. and Poulain, Tanja and Pramstaller, Peter P. and Preuss, Michael H. and Prins, Bram P. and Province, Michael A. and Rabelink, Ton J. and Raffield, Laura M. and Raitakari, Olli T. and Reilly, Dermot F. and Rettig, Rainer and Rheinberger, Myriam and Rice, Kenneth M. and Ridker, Paul M. and Rivadeneira, Fernando and Rizzi, Federica and Roberts, David J. and Robino, Antonietta and Rossing, Peter and Rudan, Igor and Rueedi, Rico and Ruggiero, Daniela and Ryan, Kathleen A. and Saba, Yasaman and Sabanayagam, Charumathi and Salomaa, Veikko and Salvi, Erika and Saum, Kai-Uwe and Schmidt, Helena and Schmidt, Reinhold and Ben Schottker, and Schulz, Christina-Alexandra and Schupf, Nicole and Shaffer, Christian M. and Shi, Yuan and Smith, Albert V. and Smith, Blair H. and Soranzo, Nicole and Spracklen, Cassandra N. and Strauch, Konstantin and Stringham, Heather M. and Stumvoll, Michael and Svensson, Per O. and Szymczak, Silke and Tai, E-Shyong and Tajuddin, Salman M. and Tan, Nicholas Y. Q. and Taylor, Kent D. and Teren, Andrej and Tham, Yih-Chung and Thiery, Joachim and Thio, Chris H. L. and Thomsen, Hauke and Thorleifsson, Gudmar and Toniolo, Daniela and Tonjes, Anke and Tremblay, Johanne and Tzoulaki, Ioanna and Uitterlinden, Andre G. and Vaccargiu, Simona and Van Dam, Rob M. and Van der Harst, Pim and Van Duijn, Cornelia M. and Edward, Digna R. Velez and Verweij, Niek and Vogelezang, Suzanne and Volker, Uwe and Vollenweider, Peter and Waeber, Gerard and Waldenberger, Melanie and Wallentin, Lars and Wang, Ya Xing and Wang, Chaolong and Waterworth, Dawn M. and Bin Wei, Wen and White, Harvey and Whitfield, John B. and Wild, Sarah H. and Wilson, James F. and Wojczynski, Mary K. and Wong, Charlene and Wong, Tien-Yin and Xu, Liang and Yang, Qiong and Yasuda, Masayuki and Yerges-Armstrong, Laura M. and Zhang, Weihua and Zonderman, Alan B. and Rotter, Jerome I. and Bochud, Murielle and Psaty, Bruce M. and Vitart, Veronique and Wilson, James G. and Dehghan, Abbas and Parsa, Afshin and Chasman, Daniel I. and Ho, Kevin and Morris, Andrew P. and Devuyst, Olivier and Akilesh, Shreeram and Pendergrass, Sarah A. and Sim, Xueling and Boger, Carsten A. and Okada, Yukinori and Edwards, Todd L. and Snieder, Harold and Stefansson, Kari and Hung, Adriana M. and Heid, Iris M. and Scholz, Markus and Teumer, Alexander and Kottgen, Anna and Pattaro, Cristian},
  title     = {A catalog of genetic loci associated with kidney function from analyses of a million individuals},
  series = {Nature genetics},
  volume    = {51},
  journal   = {Nature genetics},
  number    = {6},
  publisher = {Nature Publ. Group},
  address   = {New York},
  organization    = {Lifelines COHort Study},
  issn      = {1061-4036},
  doi       = {10.1038/s41588-019-0407-x},
  pages     = {957 -- +},
  year      = {2019},
  abstract  = {Chronic kidney disease (CKD) is responsible for a public health burden with multi-systemic complications. Through transancestry meta-analysis of genome-wide association studies of estimated glomerular filtration rate (eGFR) and independent replication (n = 1,046,070), we identified 264 associated loci (166 new). Of these,147 were likely to be relevant for kidney function on the basis of associations with the alternative kidney function marker blood urea nitrogen (n = 416,178). Pathway and enrichment analyses, including mouse models with renal phenotypes, support the kidney as the main target organ. A genetic risk score for lower eGFR was associated with clinically diagnosed CKD in 452,264 independent individuals. Colocalization analyses of associations with eGFR among 783,978 European-ancestry individuals and gene expression across 46 human tissues, including tubulo-interstitial and glomerular kidney compartments, identified 17 genes differentially expressed in kidney. Fine-mapping highlighted missense driver variants in 11 genes and kidney-specific regulatory variants. These results provide a comprehensive priority list of molecular targets for translational research.},
  language  = {en}
}